2005 Fiscal Year Final Research Report Summary
Molecular mechanism of Guillain-Barre syndrome after Campylobacter jejuni enteritis : approach from bacterial analysis
| Project/Area Number |
16390254
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Dokkyo Medical University |
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Principal Investigator |
YUKI Nobuhiro Dokkyo Medical University School, Department of Neurology, Associate Professor, 医学部, 助教授 (60285913)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Michiaki Dokkyo Medical University School, Department of Neurology, Professor, 医学部, 教授 (80199702)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Guillain-Barre syndrome / Campylobacter jejuni / Lipo-oligosaccharide / Molecular mimicry |
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| Research Abstract |
Guillain-Barre syndrome (GBS), a post-infectious autoimmune-mediated neuropathy, is a serious complication after Campylobacter jejuni enteritis. To investigate the bacterial risk factor for developing GBS, genotypes, serotypes and ganglioside-mimics on lipo-oligosaccharide (LOS) were analyzed in the isolates from Japanese patients. GBS isolates more frequently were grouped in LOS biosynthesis locus class A (72/106 ; 68%) than were enteritis isolates (17/103 ; 17%). Class A strains predominantly had genotype cst-II (Thr51), which is responsible for biosynthesis of GM1- and GD1a-like LOSs. Indeed we found that strains with cst-II (Thr51) regularly expressed the GM1 and GD1a epitopes, whereas those with cst-II (Asn51) had the GQ1b epitope. Patients who had C.jejuni (Thr51) more frequently were positive for anti-GM1 and anti-GD1a IgG and had limb weakness. Patients infected with C.jejuni (Asn51) more often were positive for anti-GQ1b IgG and had ophthalmoparesis and ataxia. Predominant cst-II genotype was Thr51 in the isolates from GBS patients, whereas it was Asn51 in those with Fisher syndrome. Class A locus clustering in GBS isolates, recently reported in Europe, provides the first GBS-related C.jejuni characteristic common to Asia and Europe. Class A locus seems to be linked to cst-II polymorphism, resulting in promotion of both GM1- and GD1a-like structure synthesis on LOS ; consequently, increasing the risk of producing anti-ganglioside antibodies and developing GBS. The genetic polymorphism of C.jejuni determines autoantibody reactivity and the clinical presentation of GBS, possibly through modification of the host-mimicking molecule.
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Research Products
(70 results)
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[Journal Article] Identification of a sialate-O-acetyltransferase from Campylobacter jejuni : demonstration of direct transfer to the C9 position of terminal α-2,8-linked sialic acid.2006
Author(s)
Houliston RS, Endtz HP, Yuki N, Li J, Jarrell HC, Koga M, van Belkum A, Karwaski MF, Wakarchuk WW, Gilbert M.
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Journal Title
J Biol Chem (Epub ahead of print)
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] Overexpression of GD1a ganglioside sensitizes motor nerve terminals to anti-GD1a antibody-mediated injury in a model of acute motor axonal neuropathy.2005
Author(s)
Goodfellow JA, Bowes T, Sheikh K, Odaka M, Halstead SK, Humphreys PD, Wagner ER, Yuki N, Furukawa K, Furukawa K, Plomp JJ, Willison HJ.
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Journal Title
J Neurosci 25 (selected for the 'This Week in The Journal' section in the issue)
Pages: 1620-1628
Description
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[Journal Article] Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome.2004
Author(s)
Yuki N, Susuki K, Koga M, Nishimoto Y, Odaka M, Hirata K, Taguchi K, Miyatake T, Furukawa K, Kobata T, Yamada M.
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Journal Title
Proc Natl Acad Sci USA 101
Pages: 11404-11409
Description
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[Journal Article] The crucial role of Campylobacter jejuni genes in anti-ganglioside antibody induction in the Guillain-Barre syndrome.2004
Author(s)
Godschalk PCR, Heikema AP, Gilbert M, Komagamine T, Ang CW, Glerum J, Brochu D, Li J, Yuki N, Jacobs BC, van Belkum A, Endtz HPh.
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Journal Title
J Clin Invest 114
Pages: 1659-1665
Description
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